Mucosal immunity to Toxoplasma gondii
Our studies comparing T. gondii infected gnotobiotic (germ-free) animals to conventional mice have established that the immunostimulatory signals induced by intestinal bacteria have major effects on the outcomes of the parasitic infections. We have revealed that lack of intestinal bacteria not only results in multiple defects in T cell activation but also results in a dramatic increase in susceptibility to the parasitic infection.
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Paneth Cells in intestinal homeostasis and inflammation
Our experiments revealed that IFN-gamma production by CD4+ Th1 cells during mucosal responses to the protozoan parasite Toxoplasma gondii triggers Paneth cell death. We are interested in identifying mechanisms of Paneth cell death and the effects on Paneth cell loss on the intestinal inflammation.
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Neutrophils in host defense and inflammation
Our lab uses a combination of cellular and molecular techniques to (i) determine the transcription factors that regulate neutrophil development and activation, and (ii) examine the effects of neutrophil-derived cytokines in the regulation of the innate and adaptive immune responses to T. gondii.
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